Abstract:

Light-at-night has become an increasing and essential part of the modern lifestyle and leads to a number of
health problems, including excessive body mass index, cardiovascular diseases, diabetes, and cancer. The International
Agency for Research on Cancer (IARC) Working Group concluded that “shift-work that involves circadian disruption is
probably carcinogenic to humans” (Group 2A) [1]. According to the circadian disruption hypothesis, light-at-night might
disrupt the endogenous circadian rhythm and specifically suppress nocturnal production of the pineal hormone melatonin
and its secretion into the blood. We evaluated the effect of various light/dark regimens on the survival, life span, and
spontaneous and chemical carcinogenesis in rodents. Exposure to constant illumination was followed by accelerated aging
and enhanced spontaneous tumorigenesis in female CBA and transgenic HER-2/neu mice. In male and female rats maintained
at various light/dark regimens (standard 12:12 light/dark [LD], the natural light [NL] of northwestern Russia, constant
light [LL], and constant darkness [DD]) from the age of 25 days until natural death, it was found that exposure to NL
and LL regimens accelerated age-related switch-off of the estrous function (in females), induced development of metabolic
syndrome and spontaneous tumorigenesis, and shortened life span both in male and females rats compared to the
standard LD regimen. Melatonin given in nocturnal drinking water prevented the adverse effect of the constant illumination
(LL) and natural light (NL) regimens on the homeostasis, life span, and tumor development both in mice and rats.
The exposure to the LL regimen accelerated colon carcinogenesis induced by 1,2-dimethylhydrazine (DMH) in rats,
whereas the treatment with melatonin alleviated the effects of LL. The maintenance of rats at the DD regimen inhibited
DMH-induced carcinogenesis. The LL regimen accelerated, whereas the DD regimen inhibited both mammary carcinogenesis
induced by N-nitrosomethylurea and transplacental carcinogenesis induced by N-nitrosoethylurea in rats. Treatment
with melatonin prevented premature aging and tumorigenesis in rodents. The data found in the literature and our observations
suggest that the use of melatonin would be effective for cancer prevention in humans at risk as a result of light
pollution.

Abstract:Light-at-night has become an increasing and essential part of the modern lifestyle and leads to a number of
health problems, including excessive body mass index, cardiovascular diseases, diabetes, and cancer. The International
Agency for Research on Cancer (IARC) Working Group concluded that “shift-work that involves circadian disruption is
probably carcinogenic to humans” (Group 2A) [1]. According to the circadian disruption hypothesis, light-at-night might
disrupt the endogenous circadian rhythm and specifically suppress nocturnal production of the pineal hormone melatonin
and its secretion into the blood. We evaluated the effect of various light/dark regimens on the survival, life span, and
spontaneous and chemical carcinogenesis in rodents. Exposure to constant illumination was followed by accelerated aging
and enhanced spontaneous tumorigenesis in female CBA and transgenic HER-2/neu mice. In male and female rats maintained
at various light/dark regimens (standard 12:12 light/dark [LD], the natural light [NL] of northwestern Russia, constant
light [LL], and constant darkness [DD]) from the age of 25 days until natural death, it was found that exposure to NL
and LL regimens accelerated age-related switch-off of the estrous function (in females), induced development of metabolic
syndrome and spontaneous tumorigenesis, and shortened life span both in male and females rats compared to the
standard LD regimen. Melatonin given in nocturnal drinking water prevented the adverse effect of the constant illumination
(LL) and natural light (NL) regimens on the homeostasis, life span, and tumor development both in mice and rats.
The exposure to the LL regimen accelerated colon carcinogenesis induced by 1,2-dimethylhydrazine (DMH) in rats,
whereas the treatment with melatonin alleviated the effects of LL. The maintenance of rats at the DD regimen inhibited
DMH-induced carcinogenesis. The LL regimen accelerated, whereas the DD regimen inhibited both mammary carcinogenesis
induced by N-nitrosomethylurea and transplacental carcinogenesis induced by N-nitrosoethylurea in rats. Treatment
with melatonin prevented premature aging and tumorigenesis in rodents. The data found in the literature and our observations
suggest that the use of melatonin would be effective for cancer prevention in humans at risk as a result of light
pollution.